A Traumatic Traveler

A 19-year-old man with Duchenne Muscular Dystrophy (DMD) presented to the Emergency Department (ED) for left knee pain after ejection from his motorized wheelchair at a low velocity. In the ED, he developed increasing respiratory distress.

When addressing a new problem in a patient with a chronic condition, it is crucial to first understand the chronic condition and then consider whether the presenting symptoms relate to that condition or stem from an unrelated inciting event.

Patients with DMD are at risk of pulmonary complications relating to their underlying disease. For instance, dysphagia and ineffective cough can predispose them to recurrent aspiration pneumonitis and/or pneumonia, whereas decreased lung compliance (from scoliosis, atelectasis, and/or pulmonary fibrosis) and respiratory muscle weakness can progress to ventilatory failure. In addition, patients with DMD are at risk for pulmonary thromboembolism in the setting of immobility. Patients with DMD may also develop congestive heart failure resulting from myocardial fibrosis and nonischemic cardiomyopathy.

The ejection from his wheelchair signals potential trauma-associated conditions that could explain his respiratory distress. Respiratory complications of blunt thoracic trauma include pulmonary contusion, pneumothorax, flail chest (resulting from fractured ribs), and acute respiratory distress syndrome (ARDS). Lower extremity injury can result in venous thrombosis and pulmonary thromboembolism. While classically associated with long bone fractures, fat embolism syndrome (FES) may rarely occur with rib fractures and soft-tissue trauma. Respiratory compromise may also result from cervical spinal cord injury or severe anemia from trauma-associated hemorrhage.

Additional past medical history included growth hormone deficiency, migraine headaches, osteoporosis secondary to chronic steroid use, cardiac fibrosis of the inferolateral wall and septum with a baseline left ventricular ejection fraction of 65%, and atrial fibrillation. His medications included calcium carbonate, vitamin D, omeprazole, lisinopril, metoprolol, prednisone, escitalopram, and testosterone. Physical examination revealed an ill-appearing obese man in respiratory distress. Temperature was 37.3°C, heart rate was 102 beats per minute (bpm), blood pressure was 110/74 mm Hg. His oxygen saturation was 93% with a respiratory rate of 25 breaths per minute while breathing ambient air. His lung sounds were clear, and his heart was without murmur. The left knee was diffusely tender to palpation without specific point tenderness. Strength was 2/5 with flexion and extension at the bilateral knees and hips and 3/5 flexion and extension at the bilateral elbows. He reported this level of weakness was his baseline. Radiographs revealed a minimally displaced Salter Harris II fracture (fracture line through the metaphysis and growth plate) of the left distal femur. His fracture was splinted early in his ED course. During his ED evaluation, the patient had acute worsening of tachycardia to 130 bpm, increased respiratory rate of 34 breaths per minute, and hypoxemia with an oxygen saturation of 83% on ambient air. He was placed on 3 L/min of oxygen via nasal cannula with improvement in his oxygen saturation to 90%. A chest radiograph was unremarkable, without evidence of pneumothorax, effusion, or pneumonia. The patient was admitted to the hospital.

The acute onset of tachypnea, tachycardia, and hypoxia, accompanied by a clear lung exam and normal chest radiograph, increases the likelihood of a pulmonary embolism. Obesity, testosterone therapy, and trauma increase his susceptibility to venous thromboembolism, while a distal femur fracture increases his risk for FES. Acute pulmonary aspiration often presents with initially absent or subtle radiographic findings. An arterial blood gas analysis would determine the presence and extent of an alveolar-arterial (A-a) gradient; a normal A-a gradient is seen in hypoventilation, while an elevated A-a gradient is seen in conditions affecting gas exchange, including pulmonary emboli and alveolar filling processes. His hypoxemia only partially corrects with supplemental oxygen, raising the possibility of capillary or anatomic shunting. Capillary shunting may occur with atelectasis, aspiration/pneumonia and pulmonary edema, whereas anatomic shunting can be intra-cardiac (eg, patent foramen ovale or septic defect) or intrapulmonary (eg, arteriovenous malformations). Patients with pulmonary emboli may also develop right-to-left shunting because of increased pulmonary vascular resistance, although hypoxemia with pulmonary emboli largely relates to ventilation/perfusion mismatch and decreased level of mixed venous blood oxygen (PvO₂).